We are studying the structures and mechanisms in the caudal brainstem underlying the muscular atonia that characterizes rapid eye movement, or paradoxical sleep (PS), using electrophysiological and behavioral methods. Small bilateral dorsolateral pontine electrolytic lesions eliminate the characteristic atonia of PS, resulting in expression of such behaviors during that state as head lifting, orienting, staring, body righting, pawing, biting, forelimb support, attack and even quadrupedal walking. Other elements of PS remain intact. Behaviors expressed in PS without atonia depend upon the exact locations of lesions. We have presented evidence indicating that at least three systems are affected by the lesions: that inhibiting spinal motor neurons, a brainstem locomotor system, and in some cats one modulating aggressive behavior. We plan to dissect further the phenomenon of PS without atonia by means of thermal, knife cut and chemical lesions and electrical and chemical stimulation. Using the mircowire single unit recording technique we shall also study noradrenergic neurons in the locus coeruleus during normal PS and PS without atonia as a follow-up to our study of serotonergic dorsal raphe cells. The latter study revealed that silence of dorsal raphe neurons in PS could, in large part, be reversed by elimination of atonia in PS, indicating that dorsal raphe silence is somehow related to motor inhibiton. We shall look for similar relationships in the locus coeruleus. We shall also test for homogeneity or heterogeneity of noradrenergic cellular activity across sleep-waking states by recording from neurons in another nucleus, A5. Our long-term interest is to understand motor control during sleep and the pathophysiology of certain sleep disorders, in particular, narcolepsy.